Anti-Apolipoprotein E antibody [E6D7] (ab1907)

Overview

• Product nameAnti-Apolipoprotein E antibody [E6D7]See all Apolipoprotein E primary antibodies ...
• Description
  Mouse monoclonal [E6D7] to Apolipoprotein E
• Tested applicationsIHC-FoFr, WB, ELISA, IP, IHC-P, IHC-Fr, ICC/IF more details
• Species reactivity
  Reacts with: Mouse, Human
  
• Immunogen

  Synthetic peptide spanning the polymorphic amino acid position 158 of ApoE.

Properties

• FormLiquid
• Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
• Storage bufferPreservative: 0.1% Sodium Azide
  Constituents: PBS
• Concentration information loading...
• Purification notesAmmonium sulfate precipitated and dialyzed tissue culture supernatant.
• Clonality Monoclonal
• Clone numberE6D7
• IsotypeIgG1
• Research Areas
  • Metabolism
  • Pathways and Processes
  • Metabolic signaling pathways
  • Lipid and lipoprotein metabolism
  • Lipid metabolism

  • Metabolism
  • Types of disease
  • Heart disease

  • Metabolism
  • Types of disease
  • Neurodegenerative disease

  • Metabolism
  • Pathways and Processes
  • Metabolic signaling pathways
  • Lipid and lipoprotein metabolism
  • Cholesterol Metabolism

  • Metabolism
  • Types of disease
  • Cancer

  • Developmental Biology
  • Lineage specification
  • Endoderm

  • Stem Cells
  • Lineage Markers
  • Endoderm

  • Cancer
  • Cancer Metabolism
  • Metabolic signaling pathway
  • Metabolism of lipids and lipoproteins

  • Signal Transduction
  • Metabolism
  • Lipid metabolism

  • Cardiovascular
  • Lipids / Lipoproteins
  • Lipid Metabolism
  • Cholesterol Metabolism

  • Cardiovascular
  • Atherosclerosis
  • Lipid transport

  • Cardiovascular
  • Lipids / Lipoproteins
  • Lipoproteins/Apolipoproteins

  • Neuroscience
  • Neurology process
  • Neurodegenerative disease
  • Other

  • Neuroscience
  • Neurology process
  • Neurodegenerative disease
  • Alzheimer's disease
  • Other

Applications

Target

• FunctionMediates the binding, internalization, and catabolism of lipoprotein particles. It can serve as a ligand for the LDL (apo B/E) receptor and for the specific apo-E receptor (chylomicron remnant) of hepatic tissues.
• Tissue specificityOccurs in all lipoprotein fractions in plasma. It constitutes 10-20% of very low density lipoproteins (VLDL) and 1-2% of high density lipoproteins (HDL). APOE is produced in most organs. Significant quantities are produced in liver, brain, spleen, lung, adrenal, ovary, kidney and muscle.
• Involvement in diseaseDefects in APOE are a cause of hyperlipoproteinemia type 3 (HLPP3) [MIM:107741]; also known as familial dysbetalipoproteinemia. Individuals with HLPP3 are clinically characterized by xanthomas, yellowish lipid deposits in the palmar crease, or less specific on tendons and on elbows. The disorder rarely manifests before the third decade in men. In women, it is usually expressed only after the menopause. The vast majority of the patients are homozygous for APOE*2 alleles. More severe cases of HLPP3 have also been observed in individuals heterozygous for rare APOE variants. The influence of APOE on lipid levels is often suggested to have major implications for the risk of coronary artery disease (CAD). Individuals carrying the common APOE*4 variant are at higher risk of CAD.
  Genetic variations in APOE are associated with Alzheimer disease type 2 (AD2) [MIM:104310]. It is a late-onset neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated in neuronal death. Note=The APOE*4 allele is genetically associated with the common late onset familial and sporadic forms of Alzheimer disease. Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE*4 alleles in 42 families with late onset AD. Thus APOE*4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE*4 was virtually sufficient to cause AD by age 80. The mechanism by which APOE*4 participates in pathogenesis is not known.
  Defects in APOE are a cause of sea-blue histiocyte disease (SBHD) [MIM:269600]; also known as sea-blue histiocytosis. This disorder is characterized by splenomegaly, mild thrombocytopenia and, in the bone marrow, numerous histiocytes containing cytoplasmic granules which stain bright blue with the usual hematologic stains. The syndrome is the consequence of an inherited metabolic defect analogous to Gaucher disease and other sphingolipidoses.
  Defects in APOE are a cause of lipoprotein glomerulopathy (LPG) [MIM:611771]. LPG is an uncommon kidney disease characterized by proteinuria, progressive kidney failure, and distinctive lipoprotein thrombi in glomerular capillaries. It mainly affects people of Japanese and Chinese origin. The disorder has rarely been described in Caucasians.
• Sequence similaritiesBelongs to the apolipoprotein A1/A4/E family.
• Post-translational
  modificationsSynthesized with the sialic acid attached by O-glycosidic linkage and is subsequently desialylated in plasma. O-glycosylated with core 1 or possibly core 8 glycans. Thr-307 is a minor glycosylation site compared to Ser-308.
  Glycated in plasma VLDL of normal subjects, and of hyperglycemic diabetic patients at a higher level (2-3 fold).
  Phosphorylation sites are present in the extracelllular medium.
• Cellular localizationSecreted.

Target information above from: UniProt accession P02649 The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010) .

Information by UniProt
• Database links
  • Entrez Gene: 348 Human
  • Entrez Gene: 11816 Mouse
  • Omim: 107741 Human
  • SwissProt: P02649 Human
  • SwissProt: P08226 Mouse
  • Unigene: 654439 Human
  • Unigene: 305152 Mouse

• Alternative names
  AD2 antibodyAlzheimer disease 2 antibodyApo E antibody

  Apo-E antibodyApoE antibodyAPOE_HUMAN antibodyAPOEA antibodyApolipoprotein E antibodyApolipoprotein E3 antibodyApolipoproteinE antibodyApoprotein antibodyLDLCQ5 antibodyLPG antibodyMGC1571 antibody

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Anti-Apolipoprotein E antibody [E6D7] images

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  Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Apolipoprotein E antibody [E6D7] (ab1907)
  Ab1907 staining Human liver. Staining is localised to cytoplasmic and extracelular regions.
  Left panel: with primary antibody at 1 ug/ml. Right panel: isotype control.
  Sections were stained using an automated system DAKO Autostainer Plus , at room temperature: sections were rehydrated and antigen retrieved with the Dako 3 in 1 AR buffers citrate EDTA pH 9.0 in a DAKO PT Link. Slides were peroxidase blocked in 3% H2O2 in methanol for 10 mins. They were then blocked with Dako Protein block for 10 minutes (containing casein 0.25% in PBS) then incubated with primary antibody for 20 min and detected with Dako envision flex amplification kit for 30 minutes. Colorimetric detection was completed with Diaminobenzidine for 5 minutes. Slides were counterstained with Haematoxylin and coverslipped under DePeX. Please note that for manual staining we recommend to optimize the primary antibody concentration and incubation time (overnight incubation), and amplification may be required.
• 

  Immunocytochemistry/ Immunofluorescence-Apolipoprotein E antibody [E6D7](ab1907)
  ICC/IF image of ab1907 stained HepG2 cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab1907, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-mouse IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
  
  
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  Immunohistochemistry (PFA perfusion fixed frozen sections) - Anti-Apolipoprotein E antibody [E6D7] (ab1907)Ruma Raha-Chowdhury, University Of Cambridge, United Kingdom
  IHC-FoFr image of Apolipoprotein E staining on choroid plexus of APP transgenic mouse brain sections using ab1907 (1:500). The mouse was perfused with 4% PFA in 0.1M PBS. The sections were permeabilised using 0.1% TriktonXin 0.1% PBS. 10% serum was used for 1 hour at 24°C for blocking step. The sections were stained using ab1907 at 1:500 dilution and Rabbit monoclonal to anti-mouse IgG conjugated to Alexa Fluor 568 was used at 1:1000 to detect the primary antibody. DAPI was used to stain the nuclei

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